Abstract

Context

Increased free fatty acids (FFAs) levels, typical in obesity condition, can contribute to systemic lipotoxicity and inflammation adversely influencing Inflammatory Bowel Disease development and progression. Anthocyanins possess health promoting properties mainly associated to the induction of Nrf2-regulated cytoprotective proteins.

Objective

Using a novel experimental model, we evaluated the in vitro intracellular mechanisms involved in FFAs modulation of intestinal epithelial lipotoxicity and the protective effects of cyanidin-3-O-glucoside (C3G) in Caco-2 cells.

Results

Caco-2 exposed to palmitic acid (PA) in the serosal (basolateral) side showed a combined state of epithelial inflammation, inducing NF-κB pathway and downstream cytokines, that was reverted by C3G apical pre-treatment. In addition, PA altered intracellular redox status and induced reactive oxygen species that were reduced by C3G via the redox-sensitive Nrf2 signalling.

Discussion and conclusion

Results suggest that anti-inflammatory properties of anthocyanins, mediated by Nrf2, could represent an interesting tool for intestinal inflammatory disorders.

中文翻译：

---

Cyanidin-3-O-glucoside 保护肠上皮细胞免受棕榈酸酯诱导的脂毒性

摘要

语境

游离脂肪酸 (FFA) 水平升高是肥胖症的典型特征，可导致全身脂肪毒性和炎症，从而对炎症性肠病的发展和进展产生不利影响。花青素具有促进健康的特性，主要与诱导 Nrf2 调节的细胞保护蛋白有关。

客观的

我们使用一种新的实验模型，评估了 FFAs 调节肠上皮脂毒性的体外细胞内机制以及 cyanidin-3-O-glucoside (C3G) 在 Caco-2 细胞中的保护作用。

结果

在浆膜侧（基底外侧）暴露于棕榈酸 (PA) 的 Caco-2 显示出上皮炎症的联合状态，诱导 NF-κB 通路和下游细胞因子，通过 C3G 顶端预处理恢复。此外，PA 改变细胞内氧化还原状态并诱导活性氧，这些活性氧通过氧化还原敏感的 Nrf2 信号被 C3G 减少。

讨论与结论

结果表明，由 Nrf2 介导的花青素的抗炎特性可能是治疗肠道炎症性疾病的一种有趣工具。